IT Band Anatomy

Let us start by refreshing our IT band anatomy. Anatomy of course should of course be the basis of all biomechanics.

The IT Band commences with insertional fibres of both Gluteus Maximus and Tensor Fascia Lata and inserts into Gerdy’s Tubercle on the lateral aspect of the tibia, passing over the lateral femoral condyle. To protect the Iliotibial Band from the lateral femoral condyle there is either a bursa (fluid filled sac) or a layer of highly innervated fat that lies underneath the distal portion of the band [1].

It is essential to remember that the Iliotibial Band is nothing more than a longitudinal fibrous reinforcement of the fascia lata and has no control over its own positioning or tone.

The IT Band is often anchored to the intramuscular septum of the femur in a variety of places (this is a natural variant of IT Band anatomy) via fascial strands which pass through the periosteum (lining of the bone), rather than merely attaching to the surface.

The tension within the IT Band will ONLY increase when the origin and/or insertion are moved further apart and we will discuss how this can occur later on.

I would therefore question what one of the most common IT Band Syndrome treatment techniques employed to tackle ITBS, foam rolling, is physiologically achieving, attempting to release a non-contractile tissue which has the tensile strength of steel and is anchored firmly to cortical bone.

What Causes The Pain of ITB Syndrome?

I’d argue that this syndrome is one of compression as opposed to friction [1].

The pain stimulus within ITBS is usually inflammatory, whereby either the bursa or fat pad is compressed against the lateral femoral condyle. This will occur whenever the IT Band is shortened by a change at either its origin or insertion.

ITB Foam Roller Exercises: Treatment for Iliotibial Band Syndrome

Common features of inflammatory pain are that it is often worse with compression (for example lying on the affected side) or is most severe first thing in the morning. It will often respond well to oral ‘Non-Steriodal Anti-Inflammatory Drugs’ (NSAIDS), which are not contraindicated in such a condition as there is no collagen based healing that needs to occur.

It is often clinically beneficial to have the region examined under real-time ultrasound scan, which will determine the need for a guided corticosteroid injection, which can provide a positive reduction in symptoms in severely irritable cases. It is here that I will point out that the dreaded foam roller can often exacerbate patients symptoms, by further increasing the compression against the lateral femoral condyle.

Biomechanical Dysfunctions

1) Hip Flexor Imbalance

One biomechanical flaw that will case a increased strain of the Iliotibial Band is Hip Flexor imbalance.

Poor Iliopsoas function will result in a compensatory firing of Tensor Fascia Lata, which has the ability to assist with hip flexion because of its anatomical lever arm [2, 3]. Over a period of time, the length of the Tensor Fascia Lata will reduce (become hypertonic), which means that the Iliotibial Band origin is moved AWAY from the insertion. A secondary consequence is a rise in the anterior hip joint forces and an excessive abduction moment, which is counteracted by an additional compensation within Adductor Longus.

An underactive Iliopsoas muscle is very common within running athletes who have a tendency to use Rectus Femoris, the main Quadricep muscle, to generate hip flexion, instead of Iliopsoas. This is an extremely common running technique flaw.

The hypertonicity of Tensor Fascia Lata can be effectively treated with targeted soft tissue release. In my opinion this is most effectively performed with a large acupuncture needle, to manipulate the myofascial restriction and release any myofascial trigger points within the muscle. However, this can also be achieved with hands-on soft tissue therapy if you prefer.

For those of you that are fans of the dreaded foam roller, please roll local to the Tensor Fascia Lata (roughly near your pocket on a pair of trousers), but remember that muscles and tendons aren’t amazed by compression either, and that you run the risk of causing Gluteus Medius tendinopathy as a result [4].

2) Dynamic Knee Valgus

The most commonly seen biomechanical flaw in the running population is dynamic knee valgus, a combination of femoral internal rotation with adduction and tibial internal rotation [5]. This will result in the insertion of the Iliotibial Band being moved AWAY from the origin. This pattern of movement was linked to patients in a recent high quality prospective study by Noehren and colleagues [6].

Dynamic knee valgus can occur as a result of several muscle imbalances but the most common pattern that I see is a weakness/inhibition of Gluteus Maximus. I feel that Gluteus Maximus is more influential than Gluteus Medius in this presentation as it is a three dimensional single joint muscle, the most powerful external rotator of the hip and the superior fibres contribute significantly to hip abduction. Gluteus Medius contributes by fixing the pelvis relative to the femur [7].

3) Contralateral Pelvic Drop

A highly relevant biomechanical flaw within ITBS is a contralateral pelvic drop. This occurs in single leg stance, with the pelvis dropping down on the non-stance leg relative to the femur in the sagittal plane.

This will result in a subsequent lift of the pelvis on the stance leg, meaning that the origin of the IT Band is being moved AWAY from the insertion. This occurs as a result of a much more specific pattern of muscle imbalance, whereby Gluteus Medius (stance) and Quadratus Lumborum / External Oblique (non-stance) fail to fix the pelvis relative to the femur.

This pattern often results in over-activity within the lateral trunk on the stance limb and can be a significant contributing factor in patients with unilateral spinal pain.

Key Points for IT Band Syndrome Treatment

The point that I would like all readers to go away with is that it is muscle imbalance, and not a “tight” IT Band that causes this common problem and that it is rehabilitation (activation/strengthening) and not compression/stretching that will cure your symptoms.

Please remember that we are not robots and not all patients will fit into these simple biomechanical boxes.

People often present with combinations of these movement patterns and certainly dynamic knee valgus can be as a result of many muscle imbalances, which I will happily elaborate on in the discussion section of the blog if the questions arise.

The challenge for clinicians is to identify them, rehabilitate them and most importantly teach the patient how to transfer what they learn in the gym to their running style.

Please do not throw out the baby with the bathwater. There is still a place for (as examples) soft tissue release of the lateral quadriceps, local anti-inflammatory agents for an acute bursa, kinesio taping (a whole other debate!) to reduce pain and facilitate improved movement; but remember that these techniques treat the symptoms and only rehabilitation of the contributing factors will result in long term improvement.

Brad is a Specialist Musculoskeletal Physiotherapist from Pure Sports Medicine in London, based in Canary Wharf. He completed his BSc in Physiotherapy at the University of Hertfordshire in 2006 and a subsequent MSc in Advanced Musculoskeletal Physiotherapy at the same university in 2011. He has experience in both the NHS and private sectors of health care alongside a career in various professional sports.

His clinical interest lies in the field of Biomechanics, Patellofemoral Pain (PFJP), Tendinopathy and other overload pathologies. Academically he is a PhD candidate at Queen Mary, University of London on the topic of hip strengthening and running re-education for PFJP.

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52 Comments

Fantastic article. I’ve lost track of the number of running and triathlon clients that I see complaining of ITB who have wasted both time and discomfort rolling up and down on a variety of foam roller torture devices to alleviate their ITB issues. This is usually rectified by a deep tissue demonstration of the importance of the TFL in their ITB suffering before beginning work to rectify the muscular & / or skeletal imbalances that have contributed to it. Nice work!

Thanks for taking the time to put this together Brad…I fully agree with the sentiment of not rolling the ITB for this type of condition, but I would suggest that manual treatments are far more effective than acupuncture alone and I steer well clear of cortizone for these conditions, even if acutely inflamed.

I have bucket loads that I could comment on about what you have presented (with reference to your references etc), but I will keep my critique (and frustrations!) very brief.

If you treat this type of injury with a focus on the stance phase alone you will never fully rehabilitate your athletes.

This type of injury is more significantly associated with the swing phase. Think about that carefully in relation to the functional anatomy of the ITB as discussed in your references. I don’t know that this is researched as such but it’s taken me many years to realise this, but then again most studies are done by masters and PHD post grad students with limited practical experience….feel free to shoot me down here, but there is just too much junk research coming out that makes it abundantly clear this is the case….some people just want their pieces of paper!

Lastly, is it a friction, compression, shearing or tension problem? It’s all of them. Again think carefully about the functional anatomy and biomechanics of those athletes that present with this condition. It might not be friction as previously hypothesized, but there will most definitely be a shearing force component that is restricted due to friction between the structures at play. By the very laws of physics this cannot be described as one or the other. To do so is to be quite ignorant.

I would like to say that your comment about research being conducted by MSc or PhD candidates is naive and largely inaccurate. Firstly, there are plenty of researchers/academics who still have a clinical caseload and also some who will have also been clinicians in the past who have decided to answer some questions by their own research rather than just reading about others doing so.

Secondly, most MSc projects are not of high enough quality to make it to publication.

Thirdly, researchers will often be in contact with a clinical setting to ensure their research is contemporary and relevant to questions being asked by the clinicians.

Your commentary on this area shows lack of insight into the process. Research, when scientific, is done by making a hypothesis and then try and disprove it. That is rigour. And if u try do it in a way to prove your theory, it is flawed from the start due to bias . Just because research doesn’t give us the answer that we look for or would justify our means, it does not warrant dismissal.

The notion that its wrong to use steroidal meds into a tissue that is highly inflammatory in this condition bears no logical rationale. It is a notoriously recalcitrant condition and we should available means to help.

My last comment is that your final paragraph doesn’t make sense to me. It fails to make a point in my opinion. You fail to commit to an idea of what is the mechanism behind the lesion other saying its a bit of everything, yet won’t accept the current concepts of compression to the fatty tissue deep to the ITB.

How refreshing to read this biomechanical analysis of ITB syndr. In my treatment sessions, involving extensive muscle testing, I often find the hip flexor weakness/imbalance you speak of where the TFL is compensatory. Glut. Med. weakness is also extremely common – and also often involves a TFL compensation feeding more tension into the ITB.

I think you’re right about contralateral pelvic drop also playing a significant role.

I can’t help but notice while at the gym that the runners often spend a lot of time rolling their ITBs but almost never any time doing exercises for hip stability.

Thank you for your comments; it’s great to exchange ideas and it’s obviously a topic you’re passionate about. It appears you think that I am suggesting that one should only focus the rehabilitation of athletes with Iliotibial Band Syndrome on biomechanical errors occurring within the stance phase of running. This is not the case, and I felt I had addressed elements of this in the ‘Hip Flexor Imbalance’ section of the blog.

Your response suggests that you believe Iliotibial Band Syndrome is linked more to the swing phase of running rather than stance. I am very interested to hear both your clinical and scientific rationale for this. I have highlighted the stance phase because both from my clinical experience and also from a research perspective, this is where I feel the majority of problems occur. In fact, some studies would suggest that there is no relationship between the biomechanics of the swing phase and ITB syndrome.

Miller et al (2007) in Gait & Posture analysed the swing phase of gait in runners to fatigue. Whilst they identified greater knee flexion angles prior to foot strike in athletes with Iliotibial Band Syndrome, the average flexion angle was only 20.6o, well below the supposed 30o range of Iliotibial Band “friction” reported by other studies.

A further point that highlights the lack of a link between the swing phase of gait and Iliotibial Band Syndrome is the fact that a higher running cadence (thus increasing volume of swing mechanics but decreasing ground contact time) is associated with an improvement in symptoms. This was described as early as 1996 by Orchard et al within the American Journal of Sports Medicine and continues to be mentioned frequently throughout the literature to date.

Swing mechanics must be addressed with regards to Iliopsoas function (hence my inclusion of Sahrmann’s work), to eradicate any rotational or ab/adduction moments within the hip flexion movement, as these aberrant movements will increase local compression because of the change in fibre tension at Gerdy’s tubercle. However, this is a small piece of the puzzle in my clinical opinion. In contrast, the research suggests that this syndrome is significantly linked to the stance phase of gait. As I suggest in the blog, Noehren et al (2007) in Clinical Biomechanics prospectively identified significantly greater hip adduction/internal rotation angles within the symptomatic group. This confirmed the results of their retrospective study from a year previous and is also supported by the abovementioned retrospective work of Miller et al (2007) and the very high quality prospective work of Hamill et al (2008) from Clinical Biomechanics.

Your second point suggested that Iliotibial Band Syndrome is one of friction. My understanding of the research is that this is not the case. Both the work of Fairclough et al (2007) from the Journal of Anatomy and Falvey et al (2010) from the Scandanavian Journal of Medicine & Science in Sport rule this out for a variety of reasons. The iliotibial band is a large continuance of the fascia lata and anchors firmly and regularly to the linea aspera, through a fascial network that passes through the periostium of the femur which prevents anterior/posterior shearing or friction forces. The pathophysiology advocated by both of these studies is one of compression of a highly innervated and vascular area of fat (previously presumed to be bursa), which is inflammatory in nature and as such will respond very well to an ultrasound guided corticosteroid injection if symptoms are preventing adequate rehabilitation.

With regards your comments around the shortcomings of both research and researchers, it is difficult to come to any consensus if people simply dismiss the research that supports or negates their methods and treatments. Research does not give us all the answers, but equally, we need to move on from the “Guru driven” approaches that previously drove our profession and use research to inform our clinical practice. Further, I think it’s important to at least be aware of that which we do that is evidence based and that which isn’t. The goal of any research is the pursuit of knowledge: without it, we simply have hunches, theories and ideas. Having said that, this piece was never intended to be an exhaustive summary of the literature, or else it would be a systematic review published in a peer reviewed journal.

The beauty of a blog, as opposed to publications in a peer-reviewed journal, is that it allows the blending of research and clinical experience. I’m sure you’d agree that as professionals we have a responsibility to ensure that the information we provide maintains this balance.

Thanks again for your contribution; I look forward to further comments – either from yourself or others!

I’ve seen many runners/triathletes with ITBFS with a Varus knee as opposed to a Valgus one. If such an individual runs with a shoe with a high medial post it can exacerbate the ITBFS further. The Varus knee may cause bow-stringing of the IT Band over the lateral femoral epicondyle.

I have found foam rollering to be one of the most valuable tools for treating ITBFS. I believe it works by releasing adhesions that are formed within the deep facial connections especially with the ITB interface with Vastus Lateralis. Foam rolling and deep massage probably help restore the slide and glide movements of the muscle and connective tissue.

The biggest contributing factor to ITBFS however is the individual’s training methods which is why I’m not only a Physio but a coach. You’ve got to give the body time to adapt to an increase in run volume – and a lot of runners/triathletes don’t get this bit right.

agree with you on the foam roller .im a sports therapist and have been treating several marathon runners with itb syndrome and have found this the most effective treatment along with deep tissue on the quads (paying most attention to vastus lateralis ) and glutes (mostly maximus ).Although most clients find work on the tfl to be uncomfortable it is essential in releasing tension caused by pelvic imbalance but this is a short term treatment and a review of bio mechanics is required to achieve a satisfactory long term out come

Hi,
I have come to this debate really late but felt it important to say that I agree with Paul Savage. In my personal experience working as a sports massage therapist for the last 16 years and having treated a lot of runners with ITB Syndrome Varus pressure on the knee joint is almost always the trigger either as Paul said because a runner is wearing shoes with too much medial/arch support causing the knee to be thrown laterally as the support blocks the natural pronation of the foot. Or because the individual runs on heavily cambered surfaces. Cambered surfaces could obviously cause a valgus effect in one knee whilst a Varus effect in the other but in my experience it is generally the knee that is on the lower side of the camber that is affected as the angle of the road forces the knee laterally.

Thanks for the responses to my comment above Brad and Fizziowizzio….my obvious intent was to spark debate here and I’m pleased with the responses you’ve both presented.

To Paul, being a coach, or at least having experienced first hand what is involved in a training program is key to successfully working with athletes with long term problems preventing them from training or competing.

Brad I’m very impressed by your passion in presenting (and taking the time to find) all the relevant findings in the literature. I think that you have now emphasized what I had hoped…..that there are too many pieces for any one study to provide a recipe for treatment, not just for ITBS, but many conditions. I wanted to highlight the swing phase as an under discussed element to ITBS….as for cadence increasing and improving symptoms, i can attest to this being true, having suffered bilateral ITBS at different times. Even though there was more ‘swing phase’ then, the difference is the increased tone in the musculature that reduced the deficiencies of my swing phase more than my stance phase, which was mechanically OK. This I’ve seen replicated in patients. As a result I will often prescribe interval running with walking in between ‘race pace’ sets rather than slow pace running, which reduces the tone again and reinforces poor mechanics. (just a piece of the puzzle of course!)

As for the research, any time you read the literature it should be read with a critical mind, not treated as gospel. It should guide your treatment approaches, but not steer them. Evidence based practice alone is impossible in my honest opinion…..there are simply too many variables in the individuals that present themselves for treatment. As for ‘Guru’ driven approaches, we still need this. Look at the upsurge in research into myofascial dysfunction, it pretty much hinges on the treatment approaches that were theorised and developed over many years by a few individuals that identified previously unconsidered methods of treatment that simply worked. The research always lags behind the clinical methods, this Fizziowizzio, I’m afraid seems to have diminished in the 12 years of my career. Hence my comments on ‘too much junk research coming out’!! I can’t recall any real ‘eureka moments’ in the literature presented by highly experienced clinicians recently. I myself pulled out of an M.Phil and declined to take a PHD offer based on the fact that I was not experienced enough clinically to research and present something defining (So I am well aware of the academic environments that physios work in and who they work with).

To validate my clinical reasoning behind steering away from Cortizone injections, is simple. Pain can steer your rehab program in the right direction. Stopping pain by any means can be a real problem with chronic sports injuries particularly. Pain helps the athlete to clearly understand what should not be done, and how to manage the pain better through various motor relearning strategies. The other aspect of it for me is a cost issue. When I want to manage acute inflammation for pain relief and improving dysfunction there are many ways that don’t require a consultation with a sports physician and the associated cost, especially if imaging is recommended before any treatment actually takes place.

Fizziowizzio, I don’t not accept current concepts of the highly innervated fatty pad being compressed, I just take them with a grain of salt. How long did we accept that it was friction before this theory came out? Take things as gospel at your own peril! If you have experienced ITBS yourself you will well know that the symptoms can be neural like, so a highly innervated structure is highly likely to be involved, when I suggest that all the mechanical elements are involved, it’s not being non-committal to anyone of them, its appreciating all the direct and resultant forces that are at play and the tissues restrictions and movements that occur as such. To think that there is no compression or no friction or no tension or no shearing (or oonly any one of these) is not understanding the laws of physics here, or at least having an overly simplified view of the anatomy as most of us were unfortunately taught at Uni – ie origins and insertions! There is some great stuff coming out now in the myofascial world (as I mentioned above) that really turn things on there head and can help you to understand clinically what is going on.

Firstly – Brad, thanks for pulling together the current evidence base surrounding ITBS, and rationalising each identified factor. This provides a great model of ‘factors not to be overlooked’ in clinical assessment and treatment of this injury – rather than a ‘treatment recipe’.

Paul, thanks for your comments. I wholeheartedly agree with your point that training methods play a huge role. As such these variables need to be understood and addressed as part of any thorough treatment / rehab / prevention plan. I’d take it a step further (as per Brad and Ellis’ comments) and spend time as a rehab coach addressing run technique, especially into fatigue.

In my experience, I’ve seen far too many athletes who have completed a course of treatment and rehab for ITBS and returned to running pain free, only to be struck down by ITBS again as they start to build their volume again using the same old dysfunctional running gait. For many triathletes and runners, the successful return to running requires the learning of a fundamentally new running gait pattern.

Brad and Ellis both make this point, in talking about increased running cadence. Naturally an increased rate of running cadence reduces contact time, and increases the ‘volume of swings’, but I don’t see that as being the end of the story…

Working with athletes to change running form after ITBS, I often get the feedback that as soon as they increase their running cadence slightly for a given speed they feel their Hamstrings engage, to help facilitate (and importantly) speed up (through knee flexion) the recovery phase of swing. This often occurs to the extent that some athletes with Hamstring weakness report Hamstring DOMS after initial technique sessions.

It’s only an anecdotal coaching observation, but I’m increasingly convinced that increasing running cadence encourages increased Hamstring engagement to achieve the improved swing mechanics required to achieve the higher cadence rate. I feel that this aspect of the recovery phase of swing is all part of the key to offloading an otherwise overactive TFL and Rec.Fem.

I have been keeping an eye on this blog with interest over the past couple of weeks. A lot of interesting debate, research and reasoning has been demonstrated throughout by all who have contributed.

Both clinicians (Brad and Ellis) in particular produce valid arguments in their rationale for how they treat this problem. I see no good reason, nor evidence for putting a roller to the ITB itself, except that it is simply just a painful task for the patient and holds nothing but a poorly conceived social and cultural belief that one is lengthening the ITB. We know that the anatomical structure of the ITB cannot be lengthened at all. Sure, the TFL (in particular) can be released which can reduce the tension in the TFL-ITB complex but no ITB lengthening or shortening in isolation occurs – it’s not contractile(!) Does it break down adhesions between the underside of the ITB and the Vastus Lateralis? It’s difficult to say, but if one were to ‘break up’ an adhesion it needs to be pulled apart/stretched, not compressed surely(?) If you’re talking of breaking up a fascial adhesions, all a roller would do is squash it against the underlying muscle belly, which itself is then being squashed into the femur – no wonder it hurts so much! I don’t see any stretching going on in this process. If one has trigger points/tight muscle tissue in the Vastus Lateralis then it could potentially help, but if this is the cause of pain, then the ITB has got nothing to do with it.

With regards to ‘is it the swing phase, or is it the stance phase’ that is the issue(?) both are valid components to be looked at by the clinician. As Brad has mentioned before there is just not enough space available in this article to go through all the complex biomechanics of a running gait. But does shear/friction force of the ITB against the underlying structures occur in a running gait – well it has to, but in combination with compression (as Brad points out). Mechanically compression strain is the process of one structure being pushed into another. It is a single plane, single-vector mechanical action (in relation to the ITB: on the underlying fatty tissue/bursa the the line of force/compression is towards the anatomical midline). When one runs (whether stance or swing phase), the limb is moving in a plane of movement which is (relatively speaking) perpendicular to this plane/vector of compression strain (i.e. anterior and posterior (flexion and extension)). Therefore there has to be (at least) two vectors acting upon it – compression strain and shear strain. If compression were to occur on its own, there could only be one plane of movement. This is to say the ITB and underlying structures would have to be still in relation to one another with compression strain occuring in one plane. Let’s not forget that Fairclough’s (2006) anatomical report was conducted on cadavers and they observed this relative compression when the knee was placed into a “position” of flexion compared with a position of full extension. It was not observed as a dynamic action. Much like the MRI’s involved were also snap-shots of the limb in a set position. (Sadly true ‘Dynamic MRI’ has yet to be invented; the current ones are still static position, just with the patient vertical – not very “dynamic” at all). In short, compression and shear have to occur. Friction is simply the force resisting these forces and for friction to occur, bodies have to be in contact (i.e. compression). More compression will increase friction but only if there is a perpendicular shear force present (try rubbing your hands together when held lightly together; now do it but pushing them firmly together – harder?). Whether this occurs during the swing phase or stance phase is for the clinician to work out through quality analysis of running style, but as is well documented, the loading forces through the limb during stance phase far exceeds that of the swing phase. In poor running biomechanics, if the TFL is over-utilised in a compensatory attempt to control contralateral pelvic drop (for example), it will make it hypertonic causing greater compression of the ITB into the underlying tissues, therefore equalling more friction. If the problem exists more so in the swing phase then it can only be that the lower limb mechanics in relation to the pelvis has been altered such that the ITB is compressing/shearing/frictioning against the underlying tissues. Although you do present a worthy discussion Ellis, you don’t actually report how this process occurs or your personal hypothesis behind it, apart from your own observation and anecdotally that your tissues were hypertonic and affecting your running mechanics (as Brad suggests is part of the problem during swing phase) i.e. your biomechanics were incorrect, evidently leading to ITB/TFL related problems. I would propose that there is under-utilisation of the (ilio)psoas in the swing phase (or that it is weak), causing compensatory over-use of TFL along with Rec Fem (especially when going from extension into flexion) to assist in hip flexion resulting in greater ITB compression/shear/friction (Brad does mention this quite clearly). Ultimately poor iliopsoas force production (in a strong muscle) comes from poor pelvic control as the poor iliopsoas has no solid anchor to pull against to then pull on the femur and independently flex the hip joint. Therefore TFL and Rec Fem are recruited to assist the action. The other explanation is that the problem lies in the stance side’s QL or lateral flexors of the trunk in that they subtly laterally flex the trunk towards the stance side to translate the centre of mass over the stance limb to cause enough longitudinal loading through the stance limb to stabilise that side to allow contralateral swing to occur; with the pelvis laterally tilted i.e. compensated trendelenberg, the hip is now adducted relative to the pelvis, lengthening the ITB/TFL complex = compression/shear/friction. If muscular tonic changes are the problem then somewhere along the lines you’ve over-recruited something, most likely to compensate for a weakness elsewhere. Also, do you prescribe interval running to allow the patient time to ultimately improve the endurance in their improved running technique?

One cannot forget the process of what is a “natural running style” for a patient; that is what is habitual. People don’t know they’re doing something wrong until they come to people like us with problems. A patient could be perfectly strong in all the correct areas, but if habitually they under or over-recruit muscles, that is a problem which we must educate out of them to get them firing the right muscles to the correct force production, and at the right time i.e. make them biomechanically more efficient and effective.

Please correct me if I am wrong or my thoughts are incorrect but with a lack of explanation it is difficult to see where your reasoning is derived Ellis. Disappointing as you appear to have a very good mechanical/biomechanical knowledge. I’m not suggesting that what you say is wrong but it would be nice to hear an explanation and rationale.

From previous comments made I have decided not to reference my comments (apart from Fairclough) to avoid the threat of being under the spell of being steered by the research world as opposed to being guided by it (no matter the quality of the research I have to be able to effectively appraise the literature to decide if the research I read is fair, well constructed, unbiased and robust enough such that I can decide that the result is one which will alter my reasoning process and ulitmately my practice in conjunction with my own anecdotal evidence; but it is too easy to just poo-poo the research world and just quote anecdotal evidence as this is one of the weakest forms of evidence, as well as frankly being a bit arrogant if you solely rely on it. If everyone solely quoted anecdotal evidence, people could quote any amount of junk to come to their decisions). At least Brad has taken the time to appraise literature to support his reasoning (I’m sure he’s wasted his time in reading junk also but this has guided him to this reasoning process). I have also left out my credentials as it has no bearing on this discussion.

I agree- foam rolling the ITB when there is an underlying muscle imbalance is a fruitless exercise. IMO foam rolling has a place – to help manage DOMs but it cannot be used to treat specific soft tissue dysfunction.

I see lots of clients who have been told they have “ITB” syndrome and have been told to stop running and to use a foam roller. Frequently the one exercise they have been told to perform is a Pilates type “clam” for glute medius. As frequently theirs is serving to exacerbate problems as its so unfunctional that it has no carry over, that its not glute med thats solely the issue and they are performing it incorrectly and hence using an already tight rectus femoris.

One of my pet hates is individuals who have been given orthotics to solve the problem.

I can find that the adductors are overactive in some clients and that soft tissue release of these along with dry needling to the ITB and addressing movement dysfunction are key.

Thanks OzPhyz for understanding me on the whole concept of it being impossible to be one force and not another, and agreed I haven’t really outlined my reasoning. Let me try to now….

For years I treated ITBS much the same as I would Patello-femoral pain, with a real emphasis on improving stance phase pretty much alone without even considering the swing phase. I would watch gait patterns intently from heel strike to toe off one side then shift my attention to the next side’s heel strike to toe off….back and forth like watching tennis…and often with ITBS, unlike PFPS, I would get someone looking great from heel strike to toe off, but they would still have pain (not as bad, but still enough to not be able to train properly). This was around the same time I was experiencing ITBS myself and when I got a colleague to release my ITB, it significantly exacerbated my symptoms. This lead me to really think a lot harder about what was actually going on with my own knees and those patients that I had treated ineffectively.

The questions I asked myself were why if two patients presented with very similar stance phase mechanics would one have lateral knee pain and the other pain under or around the patella? It became a little clearer when I got the same colleague who released my ITB to do some simple manual muscle testing on me. My glutes were firing well and were strong, my rec fem was very flexible, ankle/calf range was good, hamstrings within normal limits, but the glaring deficiency was in my hip flexor strength. It was just an isometric test but it was significantly weaker on my affected side and so would have to be the one thing that I was missing in my patient’s and my own rehab. I began looking more specifically then at what these ITBS patients were doing and it was clear that they were flexing the hip and lifting through with TFL, effectively picking up the leg with the anterior portion of the ITB, not picking the leg up through the patella complex. This was then a real challenge to the concept of ‘over active’ hip flexors that should be ‘switched off’ as many therapist were advocating and still do when they encounter a Psoas that is dysfunctional. I always now strengthen hip flexors, but only once I have glutes firing well.

To tie in James’ discussion on better heel lift with the hamstrings, to do so is to change the centre of mass of the leg such that the weight of the leg produces less torque at the hip…perfect for a weak hip flexor then! This will certainly be one of the reasons why modifying running technique will reduce stress in the knee during the swing phase as well as the stance phase.

To get back to answering the question posed by OzPhyz though, what I believe in contributing to ITBS is actually a traction force created by the weight and momentum of the lower leg through the lateral structures of the knee, particularly when the femur and tibia are internally rotated more (as discussed in a lot of the papers as probably causing more tension in the ITB…..albeit in stance phase, I don’t see why this would be any less of a problem in swing phase even if there is less force involved). Some of these structures will be neural which will fit in with the concept of the highly innervated fat pad being the actual source of pain. The symptoms described (and felt by myself) are very neural in nature (burning almost) and as for most neural pain, the inhibition response of the body makes it nearly impossible to continue running……patients with PFPS can usually ‘run through’ the pain, not that I would ever condone that though!! So as part of my rehab programs I also do a lot of neural stretches and interfacing techniques.

So I think to summarise a bit to finish, a good stance phase is imperative to a good swing phase, it was never my argument that the stance phase isn’t important in ITBS, but the swing phase is the under discussed element that I personally feel is the most easily missed, or even dismissed, when treating anyone with ITBS.

Very interesting discussion and debate. Regarding the friction vs. compression issue, in contrast to what Fairclough observed, a study by Muhle et al (1999) using MR imaging showed that the IT band did in fact move posterior to the femoral epicondyle during knee flexion. Even being attached to the femur proximal to the epicondyle, it seems plausible that the length of the band running from that attachment to Gerdy’s tubercle would still be permitted anterior-posterior movement, so I don’t think this should be ruled out as a possible cause. But then there is the question that Brad raised about whether the knee flexion angle is great enough with running to be considered a problem.

It’s possible that both compression and friction forces are involved, but there are still a lot of unknowns, and I think both should still be considered when investigating the cause of the injury.

Thanks for the replies and thanks Ellis for clarifying your reasoning. However if you read back Brad clearly mentions this in his article during the swing phase (Point 1 of Biomechanical Dysfunctions).

Definitely James the ITB has to move anterior and posterior in relation to the underlying structures (bones, bursa, muscle, fatty tissue) during a normal gait cycle of swing and stance. Brad’s thoughts are that during stance there is not enough (or should not be enough) knee flexion on impact to cause this anterior-posterior shear strain to the amount you describe from Muhle’s 1999 article (that is in someone with normal pelvic control, without pelvic drop). I do agree with this. But if proximally they are not controlled, or psoas is under-recruited or weak then funny things start to happen during swing and stance, TFL then becomes recruited to assist in stabilising (in stance) or moving/flexing the hip (in swing) then the possibility of shortening in the ITB-TFL complex is increased, causing more compression, and arguably more (dare we say it) “friction” due to the normal shear strain that has to take place place (but to a minor amount). Friction is the force resisting two opposed surfaces. If you have the presence of compression, in combination with a perpendicular (shear strain) force you get friction.

Now we could discuss this all day, but I don’t think a clear conclusion will be met as we simply don’t know. Does it concern me? Frustrate me? Bug me? Not at all as this discussion is (in my opinion) aiming to debunk the common misconceptions and management of ITB friction/compression syndrome. What this is more so doing is highlighting to clinicians reading this, that biomechanical analysis is a must for this condition, and what we have highlighted are all the potential biomechanical faults that one could look out for in stance and swing phases. Rollering the ITB itself is just pointless, painful and frankly serves no purpose – it does not stretch the ITB (it itself does not get tight) and one simply cannot “release it”. Although I think Ellis is correct, he has simply gone round the houses and reiterated what Brad had said in the first place with regards to recruitment of TFL to assist weak iliopsoas/hip flexion (Point 1. Hip Flexor Imbalance!) . Why it took so many replies to establish this…..

All is all, a very good article Brad, backed up with solid scientific evidence; something that our profession governs from us, and how we should endeavour to practice with the best available evidence and knowledge. Forming untested anecdotal hypotheses is not best practice and can be dangerous in certain scenarios; it’s not scientific, it’s bad practice and is indicative of idleness. Anyone can come up with a hypothesis – like the person who once though that the world was flat, or who thought you could a) stretch the ITB itself or b) “release it” with a foam roller. Has anyone ever found scientific evidence for rollering the ITB to actually achieve these specific changes? I doubt it [FYI, a quick Pubmed search with key terms “ITB, iliotibial band, roller, foam, stretch” comes back with absolutely nothing]. Therefore a cultural socialisation of this belief has taken place somewhere and it sadly got stuck. We need to use the evidence and quality clinical reasoning to dispel things like this to improve our practice and stop gym goers across the land from experiencing excruciating pain at the hands of the foam roller for zero gain. Unless they have some strange perversion to it, in which case carry on.

Any clinicians following this discussion I would suggest you start addressing muscle imbalance sooner rather than later and analysing running/gait biomechanics and movement patterns (with a slow-motion camera – anyone purporting to be able to do this with the naked eye, real time, is lying). In short, everything is biomechanics(!)

I hope that someone can take this discussion now and run with it and maybe even look at some of the ideas presented here in more detail in a research project that can give us our ‘Eureka’ moment!

One last thing that I have noticed with people suffering ITBS vs PFPS….purely anecdotal of course….is that ITBS sufferers tend toward hypermobility where as PFPS suffers do not. Just one more thing to ponder!

Apologies for my delay in replying but this has allowed an interesting debate to take shape.

Paul – I 100% agree with your comments with regards to training volumes, this is an overriding factor in so many patients’ presentations in a variety of pathologies. I think that the weakness versus inhibition debate always requires a 3rd arm and that is one of fatigue. With regards to Vastus Lateralis, so many athletes are dominant through their lateral and central Quadriceps because of the moderate range of motion that they train within, but I would not choose to employ a foam roller as my tool of choice to combat this. The overall answer is to ensure that athletes complete a full range of motion in their strength & conditioning training, my favourites being either a full front/back squat below 90 degrees (with good form), or a variation of a split squat.

Claire – again I agree with your sentiments with regards to Gluteus Medius, the clam simply is not an exercise for this muscle. I would encourage you not to abandon this exercise completely, it can be very useful to teach trunk/pelvis disassociation or if patients present with an under-activity within their short rotators but clinically this is so rare. I must disagree with you with regards to orthotics, please remember that femoral/tibial adduction and internal rotation (dynamic knee valgus) is coupled with talus adduction and inversion/calcaneal eversion and sometimes navicular drop. Whilst this may not need an orthotic for correction all the time, it is essential to remember that all lower limb movements are coupled together. Certain patients’ biomechanical dysfunction can be what I describe as ‘bottom up’ (foot driven) and the skilled clinician will identify this group and should send them to an excellent musculoskeletal podiatrist. Look at Barwick et al (2012) in the Foot Journal for an excellent review of how foot motion couples with lumbopelvic-hip mechanics. Please do not confuse this with the grossly erroneous term ‘overpronation’ and if you haven’t done so already, take the time to read this excellent summary by my colleague Ian Griffiths.

Ellis – I am still struggling to understand quite why you felt it necessary to raise the importance of swing mechanics within this blog in such a fashion, as I felt (and it seems from other reader’s comments) that I had done an adequate job of stressing this within the main body of text. I would completely agree with you that hip flexor dysfunction and/or swing phase mechanics are often undervalued and I would implore you all to look towards Shirley Sahrmann’s work on Iliopsoas dysfunction; this is what I base my arguments on when it comes to this area. I do not think that we see many “tight” hip flexors clinically, but more so an underactive Iliopsoas that is causing an overactive Rectus Femoris/Tensor Fascia Lata/Adductor Longus to name but a few.

Again Ellis I would like to reiterate that your so-called ‘eureka’ moment is there for you within the evidence base, whilst not everything within our profession is backed up by Level I evidence, expert clinicians that feel they are ahead of the research must at least have supplementary evidence for what they do clinically, and certainly must present it when engaging in debate with other professionals. As Oz Phys states very well, I am not blindly guided by the evidence base, but you must evaluate, appraise thus decide what you will follow and what you will dismiss.

James S/Oz Phys – thank you for your support and kind comments. I fully appreciate that Fairclough’s work is cadaveric in nature and I believe that he and his team made an excellent decision in backing this up with MRI imaging to increase the clinical applicability. These results are supported by a follow up piece of work by Falvey et al within the Scandanavian Journal of Medicine & Science in Sports (2010, 20 (4), 580-587), who used real-time ultrasound scanning as opposed to MRI, the obvious advantage being that this is dynamic. I would suggest therefore, if we want to go down a Physics route and describe friction as the result of two opposing forces, that we should describe non-compression force within the Iliotibial Band as “static friction” (stiction), as opposed to true “kinetic friction”? Would this be fair? I merely want to move away from patients/clinicians thinking that the pain stimulus within Iliotibial Band syndrome comes from a “rubbing” action across the Lateral Femoral Condyle and that instead compression is the driving force behind their symptoms. I could not agree more with regards to muscle imbalance and biomechanics being the main contributing factor behind all musculoskeletal injury and patients must learn to apply what we teach them clinically to whatever their functional activity, be it their running gait or their golf swing. All part of the fun and the challenge!

Well done on your comments back to everyone Brad. Thorough to say the least.

With regards to the studies which you have described and your proposal of a “non-compressive” or “static friction” force, i’m not sure if this can actually exist…. Also the physicists and biomechanists across the land may fancy a ruck on this. Friction is essentially the result of compression and although I do not wholly support the notion that friction is the culprit for this problem, I do feel that compression IS the bigger problem. In this example, the more compression present (of ITB on fat pad etc) combined with the natural shear strain during kinetic movement WILL result in more “kinetic friction”. You can’t stop friction, it is a normal phenomenon occuring all over the body between interfacing surfaces (and there are a lot of them); it is just that the inner workings of our body are, on the whole wet, relatively smooth, and interfacing surfaces lubricated by water, tissue fluid, fascia etc, hence reducing the resistive “friction” coefficient (I use the comparative of wet soapy hands vs dry hands rubbed together). “Static friction” is basically the friction force required to stop two bodies moving relative to one another (sadly the physics world decided not to refer to it as stiction).

For me what this article highlights two major points:
i) the greater problem of ITBS is COMPRESSION (but because it results in more kinetic friction = irritation). Correct faulty biomechanics/mm imbalance to prevent this compression and you should relieve friction forces
ii) the cultural, social and habitual use of a foam roller is totally pointless and totally unfounded for this problem and that we should STOP prescribing it for this problem – we’ve already established that the ITB unequivocally does not stretch, and compressing it against the femur certainly won’t stretch or release it. I have never believed in the foam roller as the theory was so poor (the scientific research even worse). I feel it is marketing and socialisation that has drawn in the therapy and fitness world to using it in this way. But now I hope we have come wise to it and will STOP this nonsense!!

Additional point iii) Fatigue hugely plays a part in performance and biomechanics. I will “fatigue train” athletes to see how their biomechanics alter under the influence of fatigue. This then guides their rehab – their biomechanics can be great, strength great but endurance lacking – just film them – essentially it highlights that all is ok but they lacking endurance fitness which puts them at risk of re-injury (especially good for ACL reconstruction athletes).

Excellent rehab point Brad and James and one that is comonly overlooked/disregarded.

Great debate guys, thoroughly interesting what everyone is putting forward.

Wondering what your thoughts are on this little theory on the impact of VL;

Over activity within an adducted hip, knee valgus on stance phase. This leads to a change in tension on ITB and thus flow on affects as discussed.
Acting like medial traction periostitis on shin – the commpartment is pressurised putting stress on surrounding structures.

Perhaps ITB roller is only releasing VL. And possible using cupping could allow break up of adhesions and allow ground substance between the facial layers to improve gliding.

Wow that was strange. I just wrote an really long comment but after I clicked submit my comment didn’t appear. Grrrr… well I’m not writing all that over again. Regardless, just wanted to say great blog!

As an itb sufferer and engineer, I would like to add that I feel my symptoms are worsened by sudden excessive training and also temperature.
The lack of articulation during exercise makes sense as does the muscle imbalance.

After a few days light, high rep, full articulation squats and warming, rubbing the side of the knee prior to training, all was fixed!

Brad, I have only just discovered this fascinating debate. Whilst I feel like the moment may have passed, I post this in the hope that you can still reply…

I can relate clinically) to everything you have said, so no issues there. I agree with you that addressing the peripheral imbalances is the way to go (great blog posts by the way).

However clinically I consistently find that there seems to be a marked difference in the “quality” of my client’s ITBs. What I mean by “quality” is that some tend to be hard, almost thickened to the touch, and others are soft, almost pliable. Tightness is a factor, but often I find that manually slackening the ITB passively doesn’t seem to change its quality (to the touch). A hardened/thickened ITB seems to remain hardened/thickened when slackened. Why is that?

Also, clinically I have found that gentle, persistent and consistent working of the ITB does seem to gradually change its quality, from hardened to softened. I understand that fascia does not stretch, so what is this change that am I feeling?

I appreciate that you cannot give explanations for what I subjectively “feel” when treating clients and it might be that it is actually all in my head, but any thoughts would be gratefully received.

im a sufferer from ITB pain. My doc didnt reognized it for years wich of course increaed t5he problem.To the point where I only run less than 1 min and the pain was too much I had to stop. Ive done rehab rolling…u name it. The best thing Ive found to deal with ITB is an ultrasound device with gel.I apply it when the pain comes back.I dont run long distance.I just like to jog 5 or 10 min 2 or 3 times a week, I bought an ITB strap that truly works.Now Im able to jog 10min without pain.
I think the foam roller seems to alliviate but in my case it gives for tenderness soreness to the area.I prefer massage releasing the UTB from my quds with my thump,rather than compress it with the tennis ball or whatever.
Now Im strenghning my glutes ,one leg drps etc.I realize that I had very weak muscles in that area cause I never had this soreness ever. So these are my 2 cents.
Oh and I dont think all those ITB stretches help at all.Its much better strech glues hamstrings and calves so the whole leg relax.I dont get improvement from ITB strech.
So I still havent cure this but Im here just to say that you can deal with this condition with an ultrasound home device and the pro tec ITB strap.You may not be able to play competitive sports or run a half marathon but you and enjoy a run and save lot of money in rehab and NSAiDs.
I also realize that wrong running/walking form and itb is a never ending circle.I realize after using the ultrasound my walking form improves when I got no pain.But when I got pain I start walking with my outter foot and low hip.

Great stuff, the foam roller cannot do anything here at all other than compress the lateral attachment of the ITB. We did quite a bit of anatomical research on this in cadavers in writing this paper http://db.tt/vtNXLVVl looking at exactly the lack of Stretch!
We commissioned this image http://db.tt/0To97p5g as traditionally as you have above it appears that the ITB is a structure in fact is merely the fascia of the leg , a little thicker but not different at all, makes the rollering even less likely to help
Andy

I’m a ITBS sufferer for over 10 years, from walking and jogging who has had some success managing their problem in the last few years. I have read many contradicting blogs and forums, referencing many convicting studies, and have had different advice from different doctors and read posts by inflicted people swearing by a particular solution with great confidence, while another post claims with equal enthusiasm that it is a complete wast of time. I’ve tried quite a few things, almost all of the advice didn’t help much for me but I seem to be able to manage the problem now.

It would be nice to have some higher quality studies, but even so, there is often a mistake to try to treat everybody the same. It would seem to make a lot of sense, that there are a lot of different issues that can lead to ITB knee pain, which may all contribue in each case in different amounts.

The only thing I know that definitely helps me improve is to slowly build up distance with jogging. Walking may also help a little. When out of condition, after a long period of little exercise, I only have to run 1km, or walk a few kilometers, before serious ITB pain, some times even much shorter. (Walking down hill will definitely be shorter) However, if I keep a routine of jogging often, even if I can’t jog very far at once before ITB pain, If I stay under that distance that causes pain, then very slowly increase my distance each week, stopping short as soon as any pain starts, then reduce my distance before increasing again. This way, I can very slowly increase my distance and begin to learn at what signs occur before the ITB starts to kick in.

Any time after even quite a short brake from jogging, I need to put my distance right back down, be very careful, and stop any session as soon as pain starts and slowly ramp up again. The problem is never cured, only managed.

Other things I have tried that may or may not help:
– Building up conditioning by cycling, or on a cross training machine does’t seem to help much. (I’ve never noticed any ITB at all from cycling, but I never go for much more then 1 hour)
– I’ve not been able to notice any noticeable improvement from targeted strength training hip inductors or any thing else like that I’ve tried. I suspect that if I have some muscles that fatigue after a few km running which contribues to the issue, then doing a few repetitions with some body weight exercise isn’t really going to do much to improve there conditioning relative to running a few km. If the problem occurs due to fatiguing from jogging the most, then may be jogging is the best way to improve conditioning.
– It is hard to tell if ITB stretches help at all, but I do them anyway just incase. I guess it is very difficult to lengthen your ITB this way. Although some people say it can’t be stretched, as I’ve herd claims of studies that it can be lengthened by doing stretching exercises.
– I really felt like rollers and massage helps me ramp up my milage a bit faster, but it is hard to be 100% certain about this. It does seem logical that, massage would loosen up the tissue, lessening any pressure or friction, or have some effect on the pain response, which might lessen inflammation.
– I’m considering giving dry needing a try, even if I am not sure there is really good evidence for it. If it can loosen my up to help train harder, then it could be a good thing.
– Mentally, shifting running style seems to help a little, but again it is hard to be 100% sure about this.
– I pronate on my right foot, but I get more ITB left knee, so I suspect that the pronation doesn’t have much effect for me. Certainly waring or not waring arch support didn’t seem to make any noticeable difference.
– I’ve tried icing after a run that was a little painful, just incase it helps, and doing a good massage session after a run that was a little tight. Who knows weather that helps or not, hard to be sure, but it sounds like a good idea and might at least give me some placebo which is better then nothing.
– After really over doing it, to the point you can’t walk the next day, a good rest is necessary to help, and rest is usually prescribed like it is the cure, however, I guess rest may not be good for any weakness that may help cause the issue to reoccur, and I am not sure how much strength exercises help, so when you start again, realise that you may have to take it very slow, but if you feel pain, that doesn’t necessarily you should completely stop and rest some more, it might be better to keep training at a very low rate. (I guess this is the point of strength exercises, but I couldn’t notice any help from them at all for me, but may be I wasn’t doing them right, or maybe they will help others)
– I suspect jogging using interval training methods is very good way to ramp distance up with out stressig the ITB too much, but it is hard to measure that. I would be interested in studies about that.

Anyway, I’d just thought I’d share my experience for people looking for help. If you have a conic problem, then you might just have to be determined to try a lot of things, and don’t expect to be able to go out and train hard, and know that patience and perseverance and ramping up as slowly as necessary might be a solution. It is worth it if the problem is so bad like mine that even walking a few km could be a problem.

For me, the problem seems guaranteed to recur anytime I jog too far for my current condition, but if I stay below that, I seem to be fine. I’m slowly learning to feel how my legs often tighten up during a jog before ITB pain occurs to start backing off the pase, or concentrating on my style, or even walk for a while.

Hy everybody,
great article that show us problems are the same in every country…
I think you could find some interest in reading this article with our point of vue, after testing 19 ultra-trailers who were suffering:http://podoxygene.com/articles/articles.php?id=5&cat=3
best wishes

Thank you for your brilliant article. I am a more or less brand new running and strenght coach. However my past career in health science has tought me the importance the scientifically sound approach. After reading a lot on ITBS I came to my own conclusion that the stretching approach was more or less useless. Hence I deal with ITBS by managing volume and strenghtening glutes. In your article you mention illiopsoas being an important contributor to the problem. I would love to ‘hear’ more about how it get deactivated and how to improve its firing and strenght.
Regards,
Nathalie

Having suffered from ITBS for a long time, it ultimately took a surgeon to fix it. Turned out that my lateral epicondolus was too prominent as such never allowing the IT band to fully recover. They released my ITB, shaved off some bone and I never looked back. Now I am several olympic, half and full Ironman races further, still pain free.

Just wanted to raise the point that sometimes surgery is the only option out and people should really consider this if things don’t clear within a reasonable time.

James and Brad
I agree it is compression. However occasionally everything fails to settle it.
With that in mind I have for a number of years been doing a small decompression
of the ITB. It is a minor procedure with quick recovery . It effectively decompresses the
highly innervated area that Fairclough refers to. Does it work ?

Yes it does . One of my runners who has suffered for years said I should
be knighted ( which was very nice if her but a bit generous) and had
the other done six weeks later.
I

Excellent article and Amen!
I see way too many people on YouTube, at the gym, running store and in my clinic who think they need to torture and destroy their IT Band with a roller or even a lacrosse ball. The problem is often elsewhere in the hip, pelvis or back and within a few visits if physical therapy the symptoms decrease significantly.
At the very least I try to teach people how to release the TFL.
Thanks for spreading the good word.
Aaron LeBauer PT, DPT, LMBT

In regards to the hip flexor imbalances as a potential cause for ITB symptoms and the compensatory rectus femoris activation, how would you know if the psoas isn’t functioning correctly and how would you remedy this? Or even glute max/med activation? It has been my personal experience, and i think you would agree, that isotonic strength of any of these muscles is not enough. So my question is how do you apply proper functioning of these muscles and activation patterns to the actual running form?

I wish I could understand this in it’s full context as it would be a great help to me I’m sure. I have a ITB injury that has been unsuccessful so far with 10 physio sessions with heat, US and Electrodes. I have been doing different exercises, but nothing involving squats or anything that I can see as building strength as none of it is weight bearing.

I live in Mexico so I fear my physio is not going to be the most up to date with the latest ideas in this area. Interestingly I have recently been diagnosed with hypothyroidism and wonder what effect this will have on my rehabilitation and my return to triathlon form. I have both pain in the knee and hip and feel restricted in movement hip-wise. My physio believes there is still inflammation in this area and this is the reason for the slow recovery, I disagree. It is now 4 weeks since my last run and I have taken a 2 week course of COX-2 NSAIDS.

I bought a foam roller but after reading this blog I am reluctant to start using it. Would it be more effective going to a specify sports physio? Can anyone point me in the right direction as I don’t want to waste money unnecessarily on physic that isn’t addressing the problem correctly.

Given that he has not posted to this thread for almost three years, I think we can safely assume that Brad is either too busy or secretly regretting he ever wrote this post. But if anyone has any new insights or opinions on the ITB or anything else related, please keep posting. I read the emails when I get them…